Overproduction or diminished removal of the amyloid β-protein (Aβ) in the brain are likely to play a key role in several aspects of Alzheimer's Disease (AD)-like pathology and other neuropathological conditions associated with deposition of Aβ in the brain. Endstage AD shows accumulation of large numbers of senile plaques composed of Aβ together with intraneuronal neurofibrillary tangles and loss of neurons and of white matter. In most cases, the development of the symptoms in AD is a very gradual process in which the earliest symptoms of memory loss are often slight and where AD can be extremely difficult to differentiate from benign forms of memory loss. However, about one out of three patients diagnosed with minimal cognitive impairment progress to frank AD in a period of two years. It appears that memory deficits precede massive cell loss and it is clear that synaptic dysfunction occurs far in advance of cellular loss. Therefore, it is important to better define the mechanisms underlying the early memory impairment and develop therapeutic interventions to minimize the progression of lesser memory deficits to more severe neurodegenerative diseases.